Colleen Kraft, MD, is a clinical professor of Pediatrics at the Keck School of Medicine of USC and an attending physician at the Children’s Hospital Los Angeles.

In this video, part 1 of a 5-part series, panelists discuss on recent advancements in pediatric food allergy and anaphylaxis management.

RX Review: Advances in Pediatric Food Allergy and Anaphylaxis Management

, Brian Schroer, MD, moderates a discussion with Colleen Kraft, MD, and Russell Traister, MD, on recent advancements in pediatric food allergy and anaphylaxis management.

Traister highlights omalizumab’s (Xolair) approval for food allergy, noting its potential for patients with multiple allergens. He also discusses the introduction of intranasal epinephrine, which offers an alternative to injectable auto-injectors. Recent data from the omalizumab trials suggest long-term tolerance benefits even after stopping treatment.

Kraft emphasizes the shift in primary care toward early introduction of allergenic foods at four to six months of age to prevent allergies. She also notes the growing role of oral immunotherapy (OIT) and non-injectable epinephrine in improving patient adherence.

Schroer underscores the movement toward personalized management, with allergists now assessing individual food tolerance thresholds. These innovations mark a shift from the traditional avoidance-only approach to a more tailored strategy that includes immune modulation and improved emergency treatment options.

 is an allergist immunologist at the Cleveland Clinic Children's Hospital. Board-certified in internal medicine, pediatrics, and allergy and immunology, Schroer serves as the moderator for this panel discussion.

 is a clinical professor of Pediatrics at the Keck School of Medicine of USC and an attending physician at the Children’s Hospital Los Angeles. In addition to these roles, Kraft is also the former president of the American Academy of Pediatrics.

 is a pediatric allergy and immunology specialist at Allegheny Health Network’s Pediatric Institute. Board-certified in allergy, immunology, and internal medicine, Traister serves as the third panelist for our discussion.

Relevant disclosures for Schroer include Genzyme, AstraZeneca, Amgen, GSK, and Sobi. Relevant disclosures for Kraft include Sanofi and Sobi. Relevant disclosures for Traister  include Abbvie.

Colleen Kraft, MD, MBA

Future Directions for Psoriasis Treatment

Video content above is prompted by the following:

Panelists discuss how the future of psoriasis treatment is evolving toward more personalized approaches with earlier biologic intervention for patients with high-impact disease regardless of body surface area, improved assessment tools that better capture disease burden, greater consideration of comorbidities and quality-of-life impacts, increased diversity in clinical trials, expanded patient education, innovative delivery systems, combination therapies, and targeted treatments for specific psoriasis phenotypes—all aimed at addressing current treatment gaps and moving closer to disease modification rather than merely symptom management.

Fabrizio Galimberti, MD, PhD

The panel concludes the discussion with key takeaways on the evolving treatment landscape for COPD.

Key Takeaways on the Evolving COPD Treatment Landscape

Video content above is prompted by the following question:

What are your key takeaways on the evolving COPD treatment landscape?

Igor Barjaktarevic, MD, PhD

In a new study led by Yale School of Medicine’s Cardiovascular Data Science (CarDS) Lab, researchers developed an artificial intelligence (AI) tool that can identify individuals at high risk of developing heart failure using electrocardiogram (ECG) images. The new tool enables earlier identification of heart failure, potentially reducing hospitalizations and premature death, the researchers said.

ECGs are noninvasive tests that measure the heart's electrical activity through electrodes placed on the skin. Since the tests are routinely performed and widely available, they provide an ideal platform for broader heart failure screening. Heart failure is a common cardiovascular disorder affecting millions of people worldwide.

Currently, identifying individuals at high risk for heart failure often relies on a series of clinical evaluations, including extensive clinical history, physical examination, and blood testing that may not be accessible in all settings, explains first author 

, a postdoctoral fellow in the CarDS Lab.

The AI-based tool represents a paradigm shift in heart failure risk stratification, he said.

“Using an image or photograph of a 12-lead ECG as its input, our model was able to accurately stratify heart failure risk across diverse populations in the United States, United Kingdom, and Brazil,” Dhingra said. “We can now predict who is at risk of developing heart failure in the future, well before they show overt symptoms.”

, assistant professor of medicine (cardiovascular medicine) and director of the CarDS Lab, emphasized the potential public health impact of the work.

“Every time a clinician obtains an ECG—a test that is already part of standard clinical care—our simple tool now offers an opportunity for screening and risk stratification for cardiovascular disease,” he said. “The broad availability of ECG technology, even where resources are limited, enables early intervention and improved outcomes for patients who might otherwise go undiagnosed.”

As part of CarDS Lab’s global focus, the AI model was validated across multiple international populations, showcasing its potential for large-scale adoption.

“We want to ensure broad and equitable implementation of AI-based health technologies in everyday practice,” Khera said. “That’s our next frontier.”

This study was funded by grants from the National Heart, Lung, and Blood Institute, the National Institute on Aging of the National Institutes of Health (NIH), as well as by the Doris Duke Charitable Foundation.

Heart failure risk stratification using artificial intelligence applied to electrocardiogram images: a multinational study

The Department of Internal Medicine at Yale School of Medicine is among the nation's premier departments, bringing together an elite cadre of clinicians, investigators, educators, and staff in one of the world's top medical schools. To learn more, visit

Dhingra LS, Aminorroaya A, Sangha V, Pedroso AF, Asselbergs FW, Brant LCC, Barreto SM, Ribeiro ALP, Krumholz HM, Oikonomou EK, Khera R

. Heart failure risk stratification using artificial intelligence applied to electrocardiogram images: a multinational study. Eur Heart J. 2025 Jan 13:ehae914. doi: 10.1093/eurheartj/ehae914. Epub ahead of print. PMID: 39804243.

Researchers at Yale School of Medicine's CarDS Lab have developed an AI tool that uses ECG images to identify individuals at high risk of heart failure. This tool allows for earlier detection, potentially reducing hospitalizations and premature deaths. The AI model was validated across diverse populations in the US, UK, and Brazil, highlighting its potential for widespread adoption. The study emphasizes the public health impact of integrating this tool into routine ECG tests, enabling early intervention and improved outcomes, even in resource-limited settings.

A new tool may enable earlier identification of heart failure, potentially reducing hospitalizations and premature death.

New AI Tool Identifies Risk of Future Heart Failure

Julia Eisen

Let’s talk about the elephant in the room. We’ve been bouncing around it a little. Let’s talk about vaccine hesitancy and how you guys address that in education standpoints as well as how that can impact vaccination compliance or resistance. What’s your language? What’s your methodology around noticing that? Do you notice it? Do people say it to you? Do you feel it? How do you work down that road to try to convince people to get a vaccine?

Wendy Wright, DNP, ANP-BC, FNP-BC, FAANP, FAAN, FNAP:

 This is my baby. This is my doctoral work, so I love this stuff. A couple of things that I want people to know is that studies are pretty clear these days that even people who are vaccine proponents now feel the need to question science and vaccines. Every provider should expect what used to be a 30-second recommendation to now take 5 minutes because people feel the need to ask the questions about it. Even though they’re going to take it, they feel the need. There’s more vaccine hesitancy out there.

The other thing is that we talked about strong recommendations. We call it presumptive vs participatory. In a study, they followed providers who asked, “How do you feel about getting your shots today?” It shouldn’t surprise you that less than 10% of people took their shots. But when the provider said, “You’re due for 2 shots today. It’s okay to give them together,” 80% of people took those vaccines.

My last point on vaccine hesitancy is that you have to be prepared that people are going to ask about it. Take a deep breath and answer their questions. There are going to be the 4% of the population who are vaccine refusers. I’ve learned from all of my research that you will never move those folks. They believe in something that none of us can even fathom, but they come up with it. If they want to believe something, they’re going to google it and find research to support their beliefs. You’re never going to move them.

It’s the movable middle that we have to focus on. That’s the 20% to 40% of the population who will go based on a trusted source, as JAM [Jacinda Abdul-Mutakabbir, PharmD] mentioned. If they trust you and you make that recommendation, they’ll listen. Focus on the movable middle. The ones who march in and say, “What vaccines do I need? Give them to me,” are a provider’s dream. “Sure, give me everything I need.” With people in the middle, we have to take a breath, meet them where they’re at, be honest with them, give them what they’re asking, and don’t go into too much detail.

 Yes. I’ve also seen people talk about how sometimes it takes more than 1 interaction with a patient to convince them. Maybe they come in and you tell them, “You need this vaccine today,” and they say, “Absolutely not.” But by the end of the appointment, they say, “Tell me more about it and I’ll think about it for next time.” We see this with patients in the clinic with other vaccines as well. “I’m not ready to get 5 vaccines today, but I’ll get 1 next time.” We think, “OK, we’ll take what we can get. Let’s just start off on the right foot.” Sometimes it takes persistence and patience, which we don’t all have at this point in the pandemic. But there are people who can be swayed if we take the time, ask them multiple times, and not give up on them.

 Yes. We use a Z code in our charts for vaccine refusal by patient or parent. That’s a signal to the nurse practitioner who sees them next that there’s been a vaccine that they didn’t get the last time, and to take a look at the note and try to follow up on that conversation.

Wendy Wright, DNP, ANP-BC, FNP-BC, FAANP, FAAN, FNAP, and Madeline King, PharmD, BCIDP, provide insight on vaccine hesitancy among patients and the importance of increasing vaccine uptake to protect against SARS-CoV-2.

Addressing Vaccine Hesitancy and Uptake for SARS-CoV-2

Madeline King, PharmD, BCIDP

Warren Alpert Medical School of Brown University.

SLEEP 2025, the 39th annual meeting of the Associated Professional Sleep Societies

, in Seattle, Marie-Rachelle Narcisse, PhD, an assistant professor of psychiatry and human behavior at the Warren Alpert Medical School of Brown University, presented on a study that found greater oral microbiome diversity was associated with 

 duration in teenagers and young adults. 

spoke with Narcisse at the meeting about the relationship between oral microbiome diversity and long sleep in 13332 US teenagers and young adults aged 16 – 26 years.

In the first half of this interview, Narcisse discussed why this relationship in teens and young adults may impact early-life health trajectories. She explained that knowing sleep influences microbiome patterns could prevent the development of several chronic diseases, such as obesity, diabetes, and mental health disorders. The greater oral microbiome diversity in patients with long sleep duration) was demonstrated by the following measures: operational taxonomic units (43.0; 95% confidence interval [CI], 22.3 – 63.72), Faith’s phylogenetic diversity (2.96; 95% CI, 1.16 – 4.76), and Shannon-Weiner index (0.64; 95% CI, 0.07 – 1.21).

In this Q&A, Narcisse addressed the unclear directionality of this association, how inflammation, immune activity, or oral disease mediate this relationship, and what longitudinal or interventional studies are needed to explore whether modifying oral microbiota could serve as a therapeutic target for sleep health.

 While your study shows association, the directionality remains unclear. Do you think longer sleep enhances oral microbiome diversity, or does a more diverse oral microbiome promote restorative sleep?

: At this stage, we can’t say which comes first. This was a cross-sectional study — meaning it was designed to detect associations, not causation. Regardless of the causal direction between oral microbiome and sleep disorders, oral microbiome diversity may serve as a potential easy access way to monitor sleep disorders. Determining the direction of this association will require carefully designed longitudinal and mechanistic studies. For now, we view this as a promising link worth deeper exploration.

 How does inflammation, immune activity, or oral disease mediate this relationship, particularly during adolescence, a critical period for both microbiome development and circadian regulation?

: Although our study was not designed to test biological mediation, previous research suggests a strong link between inflammation, immune signaling, and changes in both sleep and the microbiome. For example, inflammatory conditions like gingivitis, common in youth, are known to alter the oral microbiome and trigger systemic cytokine release. These immune responses can interfere with circadian rhythms and sleep architecture. 

Adolescents are especially sensitive to such disruptions due to hormonal changes. Therefore, inflammation may be a key mediator in this sleep–microbiome relationship, though more targeted research is needed.

 What are the potential clinical or preventative implications that should prompt sleep specialists or pediatricians to begin thinking about oral health and microbiome diversity in the context of sleep counseling?

: Oral health is a window into whole-body health. The oral microbiome diversity could serve as a low-cost, noninvasive marker for monitoring sleep health — particularly in adolescents and young adults. 

A simple salivary microbiome profile might one day inform sleep assessments or identify youth at risk for sleep-related conditions. Promoting healthy sleep and oral hygiene together may offer synergistic benefits, especially during formative years.

 What kinds of longitudinal or interventional studies are needed to explore whether modifying oral microbiota could serve as a therapeutic target for sleep health?

: Future research should begin with longitudinal studies to track how changes in sleep patterns affect oral microbiota over time and vice versa. These should include larger, more diverse cohorts to ensure generalizability. 

Before interventional studies, the direction of causality will need to be determined, and if oral microbial dysbiosis causes sleep disorders, then improving overall oral /dental hygiene will help alleviate the sleep disorders. Intervention trials (e.g., improving oral hygiene, or modulating oral microbiota with probiotics) to observe the impact on sleep outcomes. Such studies could open new, non-invasive paths for supporting sleep health in youth.

Marie-Rachelle Narcisse, David Barker, Tsute Chen, Evangelia Morou, Kiara Medeiros, Mary Carskadon, 0360 Associations of Sleep and Oral Microbiome Among Adolescents and Young Adults in the United States, 

, Volume 48, Issue Supplement_1, May 2025, Page A157, 

https://doi.org/10.1093/sleep/zsaf090.0360

Research presented at SLEEP 2025 highlights a study linking greater oral microbiome diversity with longer sleep duration in teenagers and young adults. The study, involving 13,332 participants aged 16-26, suggests that understanding this relationship could influence early-life health trajectories and potentially prevent chronic diseases. While the study shows an association, the directionality remains unclear, necessitating further longitudinal and mechanistic studies. The potential for oral microbiota as a therapeutic target for sleep health is discussed, with future research needed to explore causality and interventional strategies.

In this Q&A, Narcisse shared what the association between greater oral microbiome diversity and longer sleep in teens and young adults could mean for early-life disease prevention.

Oral Microbiome Diversity Links to Longer Sleep, With Marie-Rachelle Narcisse, PhD

Marie-Rachelle Narcisse, PhD

Peter Miller, MD, PhD, Assistant Professor of Medicine at Massachusetts General Hospital and Harvard Medical School, is conducting groundbreaking research to elucidate the role of clonal hematopoiesis (CH) in chronic obstructive pulmonary disease (COPD), with a particular emphasis on somatic mutations in the 

 gene. COPD, a progressive lung disease resulting in airflow limitation, remains a leading cause of morbidity and mortality and is the fourth leading cause of death in the United States.

Though advancing treatment options have improved outcomes in individuals with COPD, prevention and risk stratification for both disease onset and progression remain unmet needs. Efforts to better define factors that contribute to the development and progression of COPD are therefore needed. The pathogenic drivers of COPD, which include both adaptive and innate immune signaling and characterized by enhanced inflammation, remain incompletely understood.

 Risk factors for developing COPD can be broadly categorized as age-related, environmental, and genetic. The strongest environmental risk factor remains cumulative cigarette smoke(CS) exposure.

 The genetic contributors for development of COPD have been almost exclusively related to germline risk, including monogenic risk alleles, such as alpha-1 antitrypsin deficiency, and polygenic risk contribution.

Recent investigations led by Dr. Miller have uncovered a previously unrecognized association between clonal hematopoiesis—characterized by somatic mutations in hematopoietic stem cells—and an increased risk of developing COPD, independent of conventional risk factors such as cigarette smoke exposure and inherited genetic variants.

CH is a very common, age-associated condition, with up to 10% of individuals by the age of 60-70 having large mutant clones in the peripheral blood.

, the third most frequently mutated gene in CH, have been identified as significant contributors to inflammatory pathways involved in COPD.

 mutations disrupt normal chromatin remodeling and gene regulation, promoting inflammatory responses in blood cells, notably macrophages. Dr. Miller's preliminary data strongly suggest that individuals harboring 

 mutations exhibit higher susceptibility to COPD.

To rigorously test and expand upon these findings, Dr. Miller's proposal integrates 2 comprehensive aims designed to address critical gaps in current knowledge. First, through extensive genetic epidemiological studies involving approximately 500,000 participants from prominent biobanks such as the UK Biobank, TOPMed, and Massachusetts General Brigham, the research will systematically quantify the association between 

-mutant CH and COPD. This analysis will pinpoint genetic modifiers, particularly inflammatory gene variants, which may intensify disease risk. The research further seeks to characterize distinct clinical COPD phenotypes associated with 

 mutations, such as frequency and severity of exacerbations and specific radiological manifestations of emphysema.

Second, leveraging cutting-edge mouse models, Dr. Miller's team will experimentally confirm these epidemiological findings and delve deeper into the mechanistic roles of 

 mutations in driving COPD pathogenesis. By engineering mice to express 

 mutations selectively in hematopoietic cells and subsequently exposing them to cigarette smoke, the team aims to closely mimic the human disease environment. Detailed analyses of emphysema severity, inflammatory responses, and cellular changes within lung tissues will be conducted using advanced methodologies like single-cell RNA sequencing. Furthermore, the therapeutic potential of inflammatory blockade will be rigorously evaluated, potentially offering innovative avenues for COPD management.

This integrated research approach uniquely positions Dr. Miller's work at the forefront of pulmonary medicine, bridging disciplines of hematology and pulmonology while utilizing state-of-the-art genetic and genomic tools to uncover novel inflammatory mechanisms in COPD. Outcomes from this study hold considerable promise for reshaping our understanding of COPD, significantly enhancing risk prediction, and opening pathways to groundbreaking preventative and therapeutic interventions.

Miller has no relevant disclosures to report.

1.Ford ES, Mannino DM, Wheaton AG, Giles WH, Presley-Cantrell L, Croft JB. Trends in the prevalence of obstructive and restrictive lung function among adults in the United States: findings from the National Health and Nutrition Examination surveys from 1988-1994 to 2007-2010. 

. May 2013;143(5):1395-1406. doi:10.1378/chest.12-1135

2.Kochanek KD, Murphy S, Xu J, Arias E. Mortality in the United States, 2016. 

3.Caramori G, Adcock IM, Di Stefano A, Chung KF. Cytokine inhibition in the treatment of COPD. 

. 2014;9:397-412. doi:10.2147/COPD.S42544

4.Hubeau C, Kubera JE, Masek-Hammerman K, Williams CM. Interleukin-6 neutralization alleviates pulmonary inflammation in mice exposed to cigarette smoke and poly(I:C). 

. Nov 2013;125(10):483-93. doi:10.1042/CS20130110

5.Grubek-Jaworska H, Paplinska M, Hermanowicz-Salamon J, et al. IL-6 and IL-13 in induced sputum of COPD and asthma patients: correlation with respiratory tests. 

. 2012;84(2):101-7. doi:10.1159/000334900

6.Hobbs BD, de Jong K, Lamontagne M, et al. Genetic loci associated with chronic obstructive pulmonary disease overlap with loci for lung function and pulmonary fibrosis. 

. Mar 2017;49(3):426-432. doi:10.1038/ng.3752

7.Sakornsakolpat P, Prokopenko D, Lamontagne M, et al. Genetic landscape of chronic obstructive pulmonary disease identifies heterogeneous cell-type and phenotype associations. 

. Mar 2019;51(3):494-505. doi:10.1038/s41588-018-0342-2

8.Moll M, Sakornsakolpat P, Shrine N, et al. Chronic obstructive pulmonary disease and related phenotypes: polygenic risk scores in population-based and case-control cohorts. 

. Jul 2020;8(7):696-708. doi:10.1016/S2213-2600(20)30101-6

9.Miller PG, Qiao D, Rojas-Quintero J, et al. Association of clonal hematopoiesis with chronic obstructive pulmonary disease. 

. Jan 20 2022;139(3):357-368. doi:10.1182/blood.2021013531

10.Jaiswal S, Fontanillas P, Flannick J, et al. Age-related clonal hematopoiesis associated with adverse outcomes. 

. Dec 25 2014;371(26):2488-98. doi:10.1056/NEJMoa1408617

11.Sperling AS, Gibson CJ, Ebert BL. The genetics of myelodysplastic syndrome: from clonal haematopoiesis to secondary leukaemia. 

. Jan 2017;17(1):5-19. doi:10.1038/nrc.2016.112

12.Abdel-Wahab O, Adli M, LaFave LM, et al. ASXL1 mutations promote myeloid transformation through loss of PRC2-mediated gene repression. 

. Aug 14 2012;22(2):180-93. doi:10.1016/j.ccr.2012.06.032

13.Fujino T, Goyama S, Sugiura Y, et al. Mutant ASXL1 induces age-related expansion of phenotypic hematopoietic stem cells through activation of Akt/mTOR pathway. 

. Mar 23 2021;12(1):1826. doi:10.1038/s41467-021-22053-y

14.Min KD, Polizio AH, Kour A, Thel MC, Walsh K. Experimental ASXL1-Mediated Clonal Hematopoiesis Promotes Inflammation and Accelerates Heart Failure. 

. Oct 4 2022;11(19):e026154. doi:10.1161/JAHA.122.026154

Dr. Peter Miller is pioneering research on the role of clonal hematopoiesis (CH) in COPD, focusing on ASXL1 gene mutations. COPD, a major cause of morbidity and mortality, lacks effective prevention and risk stratification strategies. Dr. Miller's work reveals a link between CH and COPD risk, independent of traditional factors like smoking. His research involves large-scale genetic studies and mouse models to explore ASXL1's impact on COPD pathogenesis. This work aims to enhance understanding of COPD, improve risk prediction, and develop novel therapeutic interventions.

Peter Miller, MD, PhD, from Massachusetts General Hospital and Harvard Medical School, is working to further uncover the role of clonal hematopoeisis in COPD.

Uncovering the Link Between Clonal Hematopoiesis and Chronic Obstructive Pulmonary Disease

Peter Miller, MD, PhD

How Climate Change is Making Your Patients' Allergies Worse

As climate change intensifies, it is not just the environment that suffers—seasonal

are getting worse, too. Global warming has led to increased droughts, wildfires, intense storms, heat waves, and rising sea levels, factors that can contribute to allergies and asthma.

According to the American Public Health Association, the 3 main causes of allergy include ambient air pollution, mold, and pollen.

 The organization also reported that 30% of adults and 40% of children experience nasal allergies.

2025 American Academy of Allergy, Asthma, & Immunology (AAAAI) 

spoke with several experts on climate change’s impact on allergies, exploring strategies clinicians can adopt to mitigate worsening allergic conditions.

, from the University of Texas Health Houston

 from Eastern Virginia Medical School at Old Dominion University

Extended Pollen Seasons and Increased Allergen Potency

Nyenhuis emphasized that pollen seasons are lengthening, especially in the western and southwestern United States, where freeze days have increased by nearly 20.

 This prolonged exposure intensifies symptoms and raises the risk of new allergies. She also noted that air pollution, particularly diesel particles, can amplify pollen’s allergenicity, worsening allergic reactions.

To help patients, Nyenhuis recommended indoor air filtration, wearing masks outdoors, and using hyper-local pollen data instead of historical weather app forecasts, which are becoming less reliable due to climate change.

Air Pollution’s Role in Allergy Development

Mahdavinia explained that air pollutants disrupt the respiratory tract’s epithelial barriers, leading to inflammation and microbiome imbalances in the nose and lungs.

 This can eliminate beneficial bacteria, allowing harmful microbes to thrive and increasing allergy risks. Mahdavinia called for expanded pollen monitoring and broader allergen testing as plant distributions shift.

Climate Change and Emerging Food Allergies

Commins discussed pollen food syndrome, in which pollen absorbed through the skin triggers food allergies.

 He also warned about the rising prevalence of alpha-gal syndrome, a meat allergy caused by tick bites. Warmer winters have expanded tick populations, increasing cases in the US, Europe, Australia, and Asia.

As climate change drives new allergy risks, clinicians must stay alert for evolving conditions such as pollen food syndrome and alpha-gal syndrome. Experts stress the importance of refining allergy diagnostics, improving access to immunotherapy, and implementing preventive strategies to protect patients in an increasingly allergenic environment.

Relevant disclosures include GlaxoSmithKline for Nyenhuis, GENZYME CORPORATION, Optinose US, Inc, and Blueprint Medicines Corporation for Mahdavinia, Regeneron Healthcare Solutions, Genetech USA, and AstraZeneca Pharmaceuticals for Commins, and Optinose US, AERIN MEDICAL, GENZYME CORPORATION, Medtronic, GlaxoSmithKline, Regeneron Pharmaceuticals, and AstraZeneca Pharmaceuticals for Lam.

. chrome-extension://efaidnbmnnnibpcajpcglclefindmkaj/https://www.apha.org/-/media/files/pdf/topics/climate/asthma_allergies.pdf. Accessed March 20, 2025.

Derman, C. Adapting Allergy Care Due to Increased Pollen Seasons, with Sharmilee Nyenhuis, MD. HCPLive. March 1, 2025. 

https://www.hcplive.com/view/adapting-allergy-care-due-increased-pollen-seasons-sharmilee-nyenhuis-md

Derman, C. How Air Pollutants Contribute to Allergies, with Mahboobeh Mahdavinia, MD, PhD. HCPLive. March 1, 2025. 

https://www.hcplive.com/view/how-air-pollutants-contribute-to-allergies-with-mahboobeh-mahdavinia-md-phd

Derman, C. Climate Change’s Impact on Allergies, with Scott Commins, MD, PhD. HCPLive. March 2, 2025. 

https://www.hcplive.com/view/climate-change-s-impact-on-allergies-scott-commins-md-phd

Climate change exacerbates seasonal allergies through increased air pollution, prolonged pollen seasons, and rising allergen potency. Experts highlight the role of air pollutants in disrupting respiratory barriers, leading to inflammation and microbiome imbalances. Emerging conditions like pollen food syndrome and alpha-gal syndrome are becoming more prevalent due to environmental shifts. Clinicians are urged to refine diagnostics, expand allergen testing, and adopt preventive strategies. The importance of using hyper-local pollen data and indoor air filtration is emphasized to mitigate allergy risks in an increasingly allergenic environment.

Climate change worsens allergies by lengthening pollen seasons, increasing air pollution, and driving new food allergies. Experts offer strategies for clinicians.

How Climate Change is Making Allergies Worse—And What Clinicians Can Do

Sharmilee Nyenhuis MD

Measuring Patient Satisfaction with Inflammatory Bowel Disease Treatments and Communication Regarding Treatment Changes 

How do you evaluate patients’ satisfaction and expectations when providing care for UC and CD?

How do you discuss with patients the idea of escalating/switching therapy, perhaps in the absence of symptoms, and target something they may not feel?

Silvio Danese, MD, PhD; Bruce Sands, MD, and Jean-Frederic Colombel, MD, conclude by sharing their approaches to evaluating patient satisfaction and expectations when providing care for ulcerative colitis and Crohn's disease, while also touching upon the importance of discussing the potential need for escalating or switching therapies to better manage the underlying disease processes. 

Silvio Danese, MD, PhD 

Syn-One Test Detects Early Parkinson Risk in REM Sleep Disorder, With Todd Levine, MD

, Todd Levine, MD, presented on a recent study that showed the Syn-One Test detected phosphorylated alpha-synuclein (P-SYN) in 75% cases of 

, he discussed the significance of these findings, how the Syn-One Test works, and how skin biopsy tests may change the diagnostic workflow for patients presenting with suspected idiopathic RBD (iRBD).

The second half of the interview focused on how early P-SYN detection may prevent the development of Parkinson Disease, dementia with Lewy bodies, and multiple system atrophy.

“The ability to identify patients with iRBD opens up the possibility for disease prevention trials,” Levine said. “There are many pharmaceutical companies targeting drugs that will lower the level of synuclein. If you wait until somebody…[has] already lost 60% of the nerves in that part of the brain… that causes Parkinson's disease. It's going to be very difficult to reverse that…But imagine now you could get to a patient 10 years before their Parkinson's disease’…This really starts to open the door for disease prevention trials.”

Levine discussed practical considerations for implementing the Syn-One Test in everyday practice. He said it is easy to incorporate. The Syn-One Test, a 3-millimeter punch biopsy, measures the presence of intra-neuronal P-SYN at the neck, around the knee, and the ankle. Mostly neurologists use the test, but sometimes internal medicine doctors and dermatologists will too.

Other tests currently used to detect P-SYN have disadvantages. For instance, DaTscans take 4 – 6 hours and often require patients to stop certain medications. The other option, spinal fluid analysis, requires patients to have spinal taps which is often disliked. The Syn-One Test offers a convenient option for patients and increases assess to the early detection of this pathological protein in patients with iRBD.

“It's not a test for every patient, but I think for many patients with REM behavior disorder, we're hearing across the country that this test really gives them an understanding of what's happening to them,” Levine said. “I think that's a critical piece of how we treat our patients in 2025.”

Relevant disclosures for Levine include Biogen, UCB, Regeneron Pharmaceuticals, Janssen Research & Development, ARGENX US, Sanofi and Genzyme US Companies, Merck KGaA, Alexion Pharmaceuticals, Mitsubishi Tanabe Pharma America, and Genentech.

Levine T, Bellaire B, Gibbons C, et al. THE SYN-SLEEP STUDY: DETECTION OF CUTANEOUS PHOSPHORYLATED ALPHA-SYNUCLEIN IN REM SLEEP BEHAVIOR DISORDER. Presented at SLEEP 2025, the 39th annual meeting of the Associated Professional Sleep Societies, in Seattle.

CND Life Sciences’ Syn-One Test® Detects Alpha-Synuclein in Skin Biopsies of Patients with REM Sleep Behavior Disorder. CND Life Sciences. June 5, 2025. https://cndlifesciences.com/syn-sleep-baseline/. Accessed June 24, 2025.

The Syn-One Test, presented by Dr. Todd Levine at SLEEP 2025, detects phosphorylated alpha-synuclein (P-SYN) in 75% of REM sleep behavior disorder (RBD) cases. This test, involving a 3-millimeter punch biopsy, offers a more convenient alternative to DaTscans and spinal fluid analysis. Early detection of P-SYN could facilitate disease prevention trials for conditions like Parkinson's disease. The test is primarily used by neurologists and provides patients with a better understanding of their condition. Levine's disclosures include associations with several pharmaceutical companies.

At SLEEP 2025, Levine discussed how skin biopsy testing for phosphorylated alpha-synuclein may enable early diagnosis and prevention trials for neurodegenerative diseases.


Authors